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dc.contributor.authorHuang, B
dc.contributor.authorWest, N
dc.contributor.authorVider, J
dc.contributor.authorZhang, P
dc.contributor.authorGriffiths, RE
dc.contributor.authorWolvetang, E
dc.contributor.authorBurtonclay, P
dc.contributor.authorWarrilow, D
dc.date.accessioned2019-11-26T03:55:56Z
dc.date.available2019-11-26T03:55:56Z
dc.date.issued2019
dc.identifier.issn1471-2334
dc.identifier.doi10.1186/s12879-019-4471-8
dc.identifier.urihttp://hdl.handle.net/10072/389276
dc.description.abstractBackground: West Nile virus (WNV) circulates across Australia and was referred to historically as Kunjin virus (WNVKUN). WNVKUN has been considered more benign than other WNV strains circulating globally. In 2011, a more virulent form of the virus emerged during an outbreak of equine arboviral disease in Australia. Methods: To better understand the emergence of this virulent phenotype and the mechanism by which pathogenicity is manifested in its host, cells were infected with either the virulent strain (NSW2012), or less pathogenic historical isolates, and their innate immune responses compared by digital immune gene expression profiling. Two different cell systems were used: a neuroblastoma cell line (SK-N-SH cells) and neuronal cells derived from induced pluripotent stem cells (iPSCs). Results: Significant innate immune gene induction was observed in both systems. The NSW2012 isolate induced higher gene expression of two genes (IL-8 and CCL2) when compared with cells infected with less pathogenic isolates. Pathway analysis of induced inflammation-associated genes also indicated generally higher activation in infected NSW2012 cells. However, this differential response was not paralleled in the neuronal cultures. Conclusion: NSW2012 may have unique genetic characteristics which contributed to the outbreak. The data herein is consistent with the possibility that the virulence of NSW2012 is underpinned by increased induction of inflammatory genes.
dc.description.peerreviewedYes
dc.languageEnglish
dc.publisherBioMed Central
dc.publisher.placeUnited Kingdom
dc.relation.ispartofpagefrom912: 1
dc.relation.ispartofpageto912: 10
dc.relation.ispartofissue1
dc.relation.ispartofjournalBMC Infectious Diseases
dc.relation.ispartofvolume19
dc.subject.fieldofresearchMicrobiology
dc.subject.fieldofresearchMicrobiology
dc.subject.fieldofresearchMicrobiology
dc.subject.fieldofresearchClinical Sciences
dc.subject.fieldofresearchMedical Microbiology
dc.subject.fieldofresearchcode0605
dc.subject.fieldofresearchcode0605
dc.subject.fieldofresearchcode0605
dc.subject.fieldofresearchcode1103
dc.subject.fieldofresearchcode1108
dc.subject.keywordsArbovirus
dc.subject.keywordsEncephalitis
dc.subject.keywordsFlavivirus
dc.subject.keywordsInflammation
dc.subject.keywordsInnate immunity
dc.titleInflammatory responses to a pathogenic West Nile virus strain
dc.typeJournal article
dc.type.descriptionC1 - Articles
dcterms.bibliographicCitationHuang, B; West, N; Vider, J; Zhang, P; Griffiths, RE; Wolvetang, E; Burtonclay, P; Warrilow, D, Inflammatory responses to a pathogenic West Nile virus strain, BMC Infectious Diseases, 2019, 19 (1), pp. 912: 1-912: 10
dcterms.dateAccepted2019-09-13
dcterms.licensehttp://creativecommons.org/licenses/by/4.0/
dc.date.updated2019-11-25T05:42:36Z
dc.description.versionPublished
gro.rights.copyright© The Author(s). 2019 Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
gro.hasfulltextFull Text
gro.griffith.authorVider, Jelena
gro.griffith.authorWest, Nic P.
gro.griffith.authorZhang, Ping


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